期刊
NATURE MEDICINE
卷 20, 期 11, 页码 1301-1309出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.3708
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资金
- Ligue Nationale contre le Cancer (Equipes labellisees)
- Site de Recherche Integree sur le Cancer (IRIC) Socrates
- ISREC Foundation
- Agence Nationale pour la Recherche (ANR AUTOPH, ANR Emergence)
- European Commission (ArtForce)
- European Research Council Advanced Investigator Grant
- Fondation pour la Recherche Medicale (FRM)
- Institut National du Cancer (INCa)
- Fondation de France
- Canceropole Ile-de-France
- Fondation Bettencourt-Schueller
- LabEx Immuno-Oncology and the Paris Alliance of Cancer Research Institutes
- Ligue Nationale contre le Cancer
- Fondation Association-pour-la-Recherche curie Cancer
- National Health and Medical Research Council (NH&MRC) Australia Fellowship
- Victorian Cancer Agency
- Associazione Italiana Ricerca contro II Cancro (AIRC) [MFAG_13058]
- Deutsche Forschungsgemeinschaft (DFG) [PF809/1-1]
- Boerhinger Ingelheim
- Association Vie et Cancer
- Institut national du Cancer et la Direction Generale de l'Offre de Soins-INSERM [6043]
Some of the anti-neoplastic effects of anthracyclines in mice originate from the induction of innate and T cell-mediated anticancer immune responses. Here we demonstrate that anthracyclines stimulate the rapid production of type I interferons (IFNs) by malignant cells after activation of the endosomal pattern recognition receptor Toll-like receptor 3 (TLR3). By binding to IFN-alpha and IFN-beta receptors (IFNARs) on neoplastic cells, type I IFNs trigger autocrine and paracrine circuitries that result in the release of chemokine (C-X-C motif) ligand 10 (CXCL10). Tumors lacking TIr3 or Ifnar failed to respond to chemotherapy unless type I IFN or Cxcl10, respectively, was artificially supplied. Moreover, a type I IFN-related signature predicted clinical responses to anthracycline-based chemotherapy in several independent cohorts of patients with breast carcinoma characterized by poor prognosis. Our data suggest that anthracycline-mediated immune responses mimic those induced by viral pathogens. We surmise that such 'viral mimicry' constitutes a hallmark of successful chemotherapy.
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